It appears that our understanding of neurons is rounded, but it is not. The advancement of the treatment of psychiatric illness is hampered because neuron-neuron interactions that cause animal behavior are poorly understood. Present-day neuron models are unlikely to advance our understanding of how neurons control behavior. These models are also unlikely to lead to the creation of animal-like robots. There are many correlations between animal behavior and levels of specific drugs, for instance. Although many physiological details are known about drug-neuron interactions, there is no mechanistic understanding of how individual neurons interact to produce normal or abnormal behavior either with or without the influence of drugs. Biological research has not yet uncovered the relationship between neuron-neuron interactions and gross features of brain function/dysfunction regarding animal behavior. Therefore, there are not clear indications of how to treat many dysfunctional behaviors. However, because of a general sense that we have a rounded understanding of the neuron and because many drug mechanisms have been highly characterized, we gravitate to drug treatments to modify problematic human interactions with an environment of things, ideas and other people. Aggression, shyness and phobia are a few problematic behaviors that psychiatrists attempt to treat with drugs. These undesirable behaviors arise from a minority of “primed circuits”, expedited pathways through chains of neurons. Using drugs, we are not able to modify problematic pathways without affecting beneficial pathways. As an example, drugs such as SSRIs, serotonin selective reuptake inhibitors, known by such brand names as PROZAC, ZOLOFT and PAXIL, are well characterized regarding physiological effects on neurons. It is believed that such drugs can lift depression. Such drugs are not selective for problematic neural circuits, but rather have a selective effect on neuron physiology throughout the brain. Because we do not know how individual neurons interact with one another to produce a normal or a depressed state, we cannot know how an SSRI modifies neuron-neuron interactions causing depression to be lifted. Similarly, neuron-neuron interactions responsible for brain pathologies, such as epilepsy and bipolar disease, remain unknown. The notion of a rounded understanding of the neuron may be inferred by some due to the abundance of “smart machines”, machines with “artificial intelligence”, pattern-recognition software and “neural networks”. It may be assumed by some that these entities have intelligence, like that, which is accepted to be a trait of animals. Therefore, one would deduce that these entities employ a known mechanism of animal neuron-neuron interaction. This is not the case. Present-day machines do not behave like animals. Intelligence devices, chiefly neural networks, which attempt to model the biological neuron, are dependent on computer hardware and software and are one-dimensional, being largely task-specific, requiring the intentional priming of pathways. Supervisory computer programs are often required to direct the behavior of these devices. Computer feedback systems that alter the functioning of these devices to suit a specific task in a specific manner are often required. These devices are static in nature rather than addressing the timing of events. Timing is of critical importance for animals in real environments. Pattern-recognition softwares, though some programs are responsive to temporal patterns, do not use a temporal mechanism to control an environment and do not attempt to model the neuron. Present-day Intelligence devices do not appear to have the ability to evolve a means of creating directed animal-like behavior in machines whether these devices are based on mechanisms used by biological neurons or not.